Apoptosis of retinoic acid resistant NB4-R1 cells induced with curcumin and its mechanism.
- Author:
Zhang-Lin ZHANG
1
;
Yun-Yuan KONG
;
La-Gen WAN
Author Information
1. Department of Laboratorial Examination, The First Affiliated Hospitul, Nanchang University, Nanchang 330006, Jiangxi Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Cell Line, Tumor;
Curcumin;
pharmacology;
Humans;
Leukemia, Promyelocytic, Acute;
metabolism;
Poly (ADP-Ribose) Polymerase-1;
Poly(ADP-ribose) Polymerases;
metabolism;
Tretinoin;
pharmacology;
bcl-X Protein;
metabolism
- From:
Journal of Experimental Hematology
2010;18(2):340-343
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to explore the inhibitory effect of Curcumin on growth of retinoic acid-resistant acute promyelocytic leukemia (APL) cells and its mechanism. The NB4-R1, an APL cell line resistant to retinoic acid, was used as a model. The growth level of NB4-R1 was detected by MTT assay, the morphologic features of cells were observed by light microscopy, the mitochondrial transmembrane potential was determined by flow cytometry, the expressions of apoptosis-related proteins procaspase 3, caspase 3, PARP and BCL-XL were measured by Western blot. The results indicated that the sensitivity of NB4-R1 to Curcumin was consistent with NB4 though NB4-R1 was resistant to retinoic acid, Curcumin displayed inhibitory effect on growth of NB4-R1 in time-and concentration-dependent manners. The morphologic observation showed existence of apoptotic bodies in NB4-R1 cells treated with 20 micromol/L of Curcumin. The flow cytometry indicated that the mitochondrial transmembrane potential in NB4-R1 cells treated with 20 micromol/L of Curcumin obviously decreased. The Western blot detection revealed that expressions of pro-caspase 3 and BCL-XL were down-regulated, expressions of caspase 3 and sheared PAPP were up-regulated in NB4-R1 cells treated with 20 micromol/L of Curcumin. It is concluded that the Curcumin can inhibit the growth and induce the apoptosis of NB4-R1.
